Nephrol Dial Transplant (2000) 15: 1517-1521
© 2000 European Renal Association-European Dialysis and Transplant Association
Editorial Comments
Acute renal failure related to the crush syndrome: towards an era of seismo-nephrology?
1 Renal Division, University Hospital, Gent, Renal Disaster Relief Task Force of the International Society of Nephrology (ISN), 2 Istanbul Medical Faculty, local coordinator for the Renal Disaster Relief Task Force, 3 Cerrahpasha Medical Faculty, President of the Turkish Society of Nephrology and 4 Renal Division, University Hospital, Gent, coordinator for the European Section of the Renal Disaster Relief Task Force
Introduction
The clinical crush syndrome occurs as a consequence of traumatic events, either accidents or disasters. In contrast to accidents, which affect only a limited number of individuals, disasters affect large numbers of victims simultaneously, thus provoking veritable crush syndrome epidemics, which often require supraregional assistance. As a result of muscular compression, myocytes are damaged, and this is followed by the release of intracellular constituents into the systemic circulation. This process is called rhabdomyolysis. One of the key compounds released is myoglobin, a 18 800 Da oxygen carrier similar to haemoglobin. In contrast to haemoglobin, however, it contains only one haeme moiety. Myoglobin is filtered by the glomeruli and reaches the tubules, where it provokes obstruction and failure of renal function [1]. Other intracellular components such as protons, phosphate, potassium, and nucleotides, i.e. precursors of uric acid, are released from the damaged muscles as well, and play an important
Pathophysiology of the muscular lesions
The role of calcium
Reperfusion injury
Compartment syndrome
Pathophysiology of ARF in rhabdomyolysis
Diagnosis
Prevention and treatment
Towards the era of seismo-nephrology
Notes
References
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